Objective: Sugar‐sweetened soft drinks contain large amounts of fructose, which may significantly increase serum uric acid levels and the risk of gout. Our objective was to evaluate the relationship between sugar‐sweetened soft drink intake, diet soft drink intake, and serum uric acid levels in a nationally representative sample of men and women.Methods: Using data from 14,761 participants age ≥20 years from the Third National Health and Nutrition Examination Survey (1988–1994), we examined the relationship between soft drink consumption and serum uric acid levels using linear regression. Additionally, we examined the relationship between soft drink consumption and hyperuricemia (serum uric acid level >7.0 mg/dl for men and >5.7 mg/dl for women) using logistic regression. Intake was assessed by a food‐frequency questionnaire.Results: Serum uric acid levels increased with increasing sugar‐sweetened soft drink intake. After adjusting for covariates, serum uric acid levels associated with sugar‐sweetened soft drink consumption categories (<0.5, 0.5–0.9, 1–3.9, and ≥4 servings/day) were greater than those associated with no intake by 0.08, 0.15, 0.33, and 0.42 mg/dl, respectively (95% confidence interval 0.11, 0.73; P < 0.001 for trend). The multivariate odds ratios for hyperuricemia according to the corresponding sweetened soft drink consumption levels were 1.01, 1.34, 1.51, and 1.82, respectively (P = 0.003 for trend). Diet soft drink consumption was not associated with serum uric acid levels or hyperuricemia (multivariate P > 0.13 for trend).Conclusion: These findings from a nationally representative sample of US adults suggest that sugar‐sweetened soft drink consumption is associated with serum uric acid levels and frequency of hyperuricemia, but diet soft drink consumption is not.

Background: Several studies have shown associations between Parkinson Disease (PD) risk and individual foods and nutrients with inconsistent results. Objective: We examined associations between dietary patterns and risk of PD in the Health Professionals Follow-Up Study (1986–2002) and the Nurses' Health Study (1984–2000). Design: We included 49 692 men and 81 676 women free of PD at baseline and used principal components analysis to identify major dietary patterns and the Alternate Healthy Eating Index (AHEI) and the alternate Mediterranean Diet Score (aMed) to assess diet quality. Relative risks (RRs) were computed by using Cox proportional hazards models within each cohort and were pooled by using a random-effects model. Results: We documented 508 new PD cases after 16 y of follow-up. The principal components analysis identified 2 dietary patterns: prudent and Western. The prudent dietary pattern, characterized by high intakes of fruit, vegetables, and fish, was inversely associated with PD risk, but the Western pattern was not. The pooled multivariate-adjusted RR for the top compared with the bottom quintiles of the prudent score was 0.78 (95% CI: 0.56, 1.07; P for trend = 0.04). For the AHEI, the pooled multivariate-adjusted RR for the top compared with the bottom quintile was 0.70 (95% CI: 0.51, 0.94; P for trend = 0.01) and for aMED was 0.75 (95% CI: 0.57, 1.00; P for trend = 0.07). Conclusions: Dietary patterns with a high intake of fruit, vegetables, legumes, whole grains, nuts, fish, and poultry and a low intake of saturated fat and a moderate intake of alcohol may protect against PD. Benefits of a plant-based dietary pattern including fish to PD merit further investigation.

Objective: To prospectively examine whether higher intakes of total flavonoids and their subclasses (flavanones, anthocyanins, flavan-3-ols, flavonols, flavones, and polymers) were associated with a lower risk of developing Parkinson disease (PD). Methods: In the current analysis, we included 49,281 men in the Health Professional Follow-up Study and 80,336 women from the Nurses9 Health Study. Five major sources of flavonoid-rich foods (tea, berry fruits, apples, red wine, and orange/orange juice) were also examined. Flavonoid intake was assessed using an updated food composition database and a validated food frequency questionnaire. Results: We identified 805 participants (438 men and 367 women) who developed PD during 20–22 years of follow-up. In men, after adjusting for multiple confounders, participants in the highest quintile of total flavonoids had a 40%lower PD risk than those in the lowest quintile (hazard ratio [HR] = 0.60; 95% confidence interval 0.43, 0.83; p trend = 0.001). No significant relationship was observed in women (p trend = 0.62) or in pooled analyses (p trend = 0.23). In the pooled analyses for the subclasses, intakes of anthocyanins and a rich dietary source, berries, were significantly associated with a lower PD risk (HR comparing 2 extreme intake quintiles were 0.76 for anthocyanins and 0.77 for berries, respectively; p trend < 0.02 for both). Conclusions: Our findings suggest that intake of some flavonoids may reduce PD risk, particularly in men, but a protective effect of other constituents of plant foods cannot be excluded.

Background: Neuroinflammation may contribute to the pathogenesis of Parkinson disease (PD). Use of nonsteroidal anti-inflammatory drugs (NSAID) in general, and possibly ibuprofen in particular, has been shown to be related to lower PD risk in previous epidemiologic studies. Methods: We prospectively examined whether use of ibuprofen or other NSAIDs is associated with lower PD risk among 136,197 participants in the Nurses9 Health Study (NHS) and the Health Professionals Follow-up Study (HPFS) free of PD at baseline (1998 for NHS and 2000 for HPFS). NSAIDs use was assessed via questionnaire. Results were combined in a meta-analysis with those of published prospective investigations. Results: We identified 291 incident PD cases during 6 years of follow-up. Users of ibuprofen had a significantly lower PD risk than nonusers (relative risk [RR], adjusted for age, smoking, caffeine, and other covariates = 0.62; 95% confidence interval [CI] 0.42–0.93; p = 0.02). There was a dose–response relationship between tablets of ibuprofen taken per week and PD risk (p trend = 0.01). In contrast, PD risk was not significantly related to use of aspirin (RR = 0.99; 95% CI 0.78–1.26), other NSAIDs (RR = 1.26; 95% CI 0.86–1.84), or acetaminophen (RR = 0.86; 95% CI 0.62–1.18). Similar results were obtained in the meta-analyses: the pooled RR was 0.73 (95% CI 0.63–0.85; p < 0.0001) for ibuprofen use, whereas use of other types of analgesics was not associated with lower PD risk. Conclusions: The association between use of ibuprofen and lower PD risks, not shared by other NSAIDs or acetaminophen, suggests ibuprofen should be further investigated as a potential neuroprotective agent against PD.